Equine metabolic syndrome is a recently described clinical disease in which horses develop insulin insensitivity similar to that described for T2DM in humans. In the same way, management of EMS in horses requires a combination of exercise and dietary modification towards a reduction in calories and a substitution of carbohydrates with fat. During exercise, the rate of ATP generated to power muscle contraction is determined by the metabolic fuel available which is either stored in the muscle or taken from the circulation. Certainly, the intensity and duration of exercise as well as diet will dictate the relative contribution of the different substrates to fuel metabolism. In horses, energy for low-intensity exercise is predominantly obtained from fat whereas energy for high-intensity exercise has a greater reliance on muscle glycogen. Although equine diets are typically high in carbohydrates and low in lipids, it has been found that chronic adaptation to fat-fortified feeds confers benefits to athletic performances of horses that may be due to enhanced 
insulin sensitivity and fat utilisation. It has further been proposed that fat-enhanced diets may also sustain or enhance other signalling functions of insulin receptors on Benzoylaconine glycolysis and lipid utilization. This possibility was supported by studies that found that the lactate threshold as well as the peak lactate increased in Arabian horses adapted to a Ginsenoside-F5 fatenhanced rather than a sugar-enhanced diet. Fat-adapted horses have been found to have faster times on the track as well as longer run times to fatigue and higher peak plasma lactate concentrations. Brown adipose tissue is distinct from white adipose tissue in its ability to expend energy and generate heat rather than as a lipid storage unit. Until recently it was thought that brown adipose tissue occurred only in mammalian infants but it is now thought that the metabolically active mitochondria-rich tissue may be retained in adults and derives from a common precursor cell for muscle. The incidence of brown adipose tissue in young horses and its persistence in adult horses, to our knowledge, have not been reported. Positive selection for genomic regions containing genes as well as two of the key determinants of brown fat cell fate, BMP7 and RB1, and their receptors and signalling molecules.